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HIV-1包膜糖蛋白gp120和gp160对富集的(CD34+)造血祖细胞体外生长的抑制作用。

Inhibitory effect of HIV-1 envelope glycoproteins gp120 and gp160 on the in vitro growth of enriched (CD34+) hematopoietic progenitor cells.

作者信息

Zauli G, Re M C, Visani G, Furlini G, La Placa M

机构信息

Institute of Microbiology, University of Bologna, Italy.

出版信息

Arch Virol. 1992;122(3-4):271-80. doi: 10.1007/BF01317189.

Abstract

The effect of increasing concentrations (from 0.01 to 10 micrograms/ml) of HIV-1 envelope glycoproteins gp160, gp120, gp41 and core protein p24 was evaluated on the in vitro growth of enriched hematopoietic progenitors (CD34+ cells). Both gp120 and gp160, at concentrations from 0.01 to 10 micrograms/ml, caused a progressive and significant (p less than 0.05) decrease in viable CD34+ cell count in liquid cultures supplemented with 2 ng/ml of human recombinant (r) interleukin-3 (IL-3), evaluated by means of Trypan-blue exclusion and [3H]thymidine ([3H]TdR) incorporation. In the absence of rIL-3, no inhibitory effects were observed even at the highest gp160 and gp120 concentrations explored (10 micrograms/ml). On the contrary, gp41 and p24 did not affect the number of viable CD34+ cells, either in the presence or in the absence of rIL-3. Moreover, gp160 and gp120, but not gp41 and p24, significantly (p less than 0.05) inhibited the in vitro growth of granulomacrophage progenitors (CFU-GM) in a dose-dependent fashion. These data clearly demonstrate that HIV-1 envelope glycoproteins inhibit the growth of purified hematopoietic progenitors. We propose that HIV-1 can impair hematopoiesis through the interaction of gp120/gp160 with CD34+ cell surface, independently of an infectious process.

摘要

评估了HIV-1包膜糖蛋白gp160、gp120、gp41以及核心蛋白p24浓度增加(从0.01至10微克/毫升)对富集造血祖细胞(CD34+细胞)体外生长的影响。通过台盼蓝排斥法和[3H]胸腺嘧啶核苷([3H]TdR)掺入法评估,在补充有2纳克/毫升人重组(r)白细胞介素-3(IL-3)的液体培养物中,浓度为0.01至10微克/毫升的gp120和gp160均导致活CD34+细胞计数逐渐且显著(p<0.05)减少。在没有rIL-3的情况下,即使在探索的最高gp160和gp120浓度(10微克/毫升)下也未观察到抑制作用。相反,无论有无rIL-3,gp41和p24均不影响活CD34+细胞的数量。此外,gp160和gp120而非gp41和p24以剂量依赖方式显著(p<0.05)抑制粒巨噬细胞祖细胞(CFU-GM)的体外生长。这些数据清楚地表明HIV-1包膜糖蛋白抑制纯化造血祖细胞的生长。我们提出HIV-1可通过gp120/gp160与CD34+细胞表面的相互作用损害造血功能,而与感染过程无关。

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